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32. Cowger J, Pagani FD, Haft JW, et al. The development of aortic insufficiency in left ventricular

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34. Salzberg SP, Lachat ML, Zünd G, et al. Left ventricular assist device (LVAD) enables survival during

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35. Feldman D, Pamboukian SV, Teuteberg JJ, et al. The 2013 Society for Heart and Lung

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36. Garan AR, Yuzefpolskaya M, Colombo PC, et al. Ventricular arrhythmias and implantable

cardioverter-defibrillator therapy in patients with continuous-flow left ventricular assist devices:

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37. Shapiro GC, Leibowitz DW, Oz MC, et al. Diagnosis of patent foramen ovale with transesophageal

echocardiography in a patient supported with a left ventricular assist device. J Heart Lung

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38. Pagani FD, Miller LW, Russell SD, et al. Extended mechanical circulatory support with a

continuous-flow rotary left ventricular assist device. J Am Coll Cardiol 2009;54:312–321.

39. Slaughter MS, Rogers JG, Milano CA, et al. Advanced heart failure treated with continuous-flow left

ventricular assist device. N Engl J Med 2009;361:2241–2251.

40. Crow S, John R, Boyle A, et al. Gastrointestinal bleeding rates in recipients of nonpulsatile and

pulsatile left ventricular assist devices. J Thorac Cardiovasc Surg 2009;137:208–215.

41. Geisen U, Heilman C, Beyeresdorf F, et al. Non-surgical bleeding in patients with ventricular assist

devices could be explained by acquired von Willebrand disease. Eur J Cardiothorac Surg

2008;33:679–684.

42. Uriel N, Pak SW, Jorde UP, et al. Acquired von Willebrand syndrome after continuous-flow

mechanical device support contributes to a high prevalence of bleeding during long-term support

and at the time of transplantation. J Am Coll Cardiol 2010;56:1207–1213.

43. Dassanayaka S, Slaughter MS, Bartoli CR. Mechanistic pathway(s) of acquired von Willebrand

syndrome with a continuous-flow ventricular assist device: in vitro findings. ASAIO J 2013;59:123–

129.

44. Eckman P, John R. Bleeding and thrombosis in patients with continuous-flow ventricular assist

devices. Circulation 2012;125:3038–3047.

45. Argiriou M, Kolokotron SM, Sakellaridis T, et al. Right heart failure post left ventricular assist

device implantation. J Thorac Dis 2014;6(suppl 1):S52–S59.

46. Aaronson KD, Slaughter MS, Miller LW, et al. Use of an intrapericardial, continuous flow,

centrifugal pump in patients awaiting heart transplantation. Circulation 2012;125;3191–3200.

47. Starling RC, Naka Y, Boyle AJ, et al. Results of the post-U.S. Food and Drug Administrationapproval study with a continuous flow left ventricular assist device as a bridge to heart

transplantation: a prospective study using the INTERMACS (Interagency Registry for Mechanically

Assisted Circulatory Support). J Am Coll Card 2011;57:1890–1898.

48. Jorde UP, Kushwaha SS, Tatooles AJ, et al. Results of the destination therapy post-Food and Drug

Administration approval study with a continuous flow left ventricular assist device. J Am Coll

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Cardiol 2014;63(17):1751–1757.

49. Miller LW, Pagani FD, Russell SD, et al. Use of a continuous-flow device in patients awaiting heart

transplantation. N Engl J Med 2007;357:885–896.

50. Park SJ, Milano CA, Tatooles AJ, et al. Outcomes in advanced heart failure patients with left

ventricular assist devices for destination therapy. Circ Heart Fail 2012;5:241–248.

51. Koval CE, Rakita R. Ventricular assist device related infections and solid organ transplantation. Am

J Transplant 2013;13:348–354.

52. Kirklin JK, Naftel DC, Kormos RL, et al. Interagency Registry for Mechanically Assisted Circulatory

Support (INTERMACS) analysis of pump thrombosis in the HeartMate II left ventricular assist

device. J Heart Lung Transplant 2014;33(1):12–22.

53. Starling RC, Moazami N, Silvestry SC, et al. Unexpected abrupt increase in left ventricular assist

device thrombosis. N Eng J Med 2014;370:33–40.

54. Goldstein DJ, John R, Salerno C, et al. Algorithm for the diagnosis and management of suspected

pump thrombus. J Heart Lung Transplant 2013;32:667–670.

55. Burkhoff D, Klotz S, Mancini DM. LVAD-induced reverse remodeling: basic and clinical implications

for myocardial recovery. J Card Fail 2006;12:227–239.

56. Birks EJ, Tansley PD, Hardy J, et al. Left ventricular assist device and drug therapy for the reversal

of heart failure. N Engl J Med 2006;355:1873–1884.

57. Guglin M, Miller L. Myocardial recovery with left ventricular assist devices. Curr Treat Options

Cardiovasc Med 2012;14(4):370–383.

58. Kantrowitz A, Tjonneland S, Freed PS, et al. Initial clinical experience with intraaortic balloon

pumping in cardiogenic shock. JAMA 1968;203:135.

59. Thiele H, Zeymer U, Neumann FJ, et al. Intra-aortic balloon support for myocardial infarction with

cardiogenic shock. N Engl J Med 2012; 367(14):1287–1296.

60. Muehrcke DD, McCarthy PM Stewart RW, et al. Extracorporeal membrane oxygenation for

postcardiotomy cardiogenic shock. Ann Thorac Surg 1996; 61:684–691.

61. Smedira NG, Wudel JH, Hlozek CC, et al. Venovenous extracorporeal life support for patients after

cardiotomy. ASAIO J 1997;43:M444–M446.

62. McGovern GJ, Magovern JA, Benckart DH, et al. Extracorporeal membrane oxygenationpreliminary results in patients with postcardiotomy cardiogenic shock. Ann Thorac Surg

1994;57:1462–1467.

63. Hill JD, O’Brien TG, Murray JJ, et al. Extracorporeal oxygenation for acute post-traumatic

respiratory failure. N Eng J Med 1972;286:629–634.

64. Gray BW, Haft JW, Hirsch JC, et al. Extracorporeal life support: experience with 2000 patients.

ASAIO J 2015;61:2–7.

65. Pagani FD, Aaronson KD, Dyke DB, et al. Assessment of an extracorporeal life support to LVAD

bridge to heart transplant strategy. Ann Thorac Surg 2000;70:1977–1985.

66. Bowen FW, Carboni AF, O’Hara ML, et al. Application of “double bridge mechanical” resuscitation

for profound cardiogenic shock leading to cardiac transplantation. Ann Thorac Surg 2001;72:86–90.

67. Smedira NG, Moazomi N, Golding CM, et al. Clinical experience with 202 adults receiving

extracorporeal membrane oxygenation for cardiac failure: survival at five years. J Thorac Cardiovasc

Surg 2001;122:92–102.

68. Thiele H, Sick P, Boudriot E, et al. Randomized comparison of intra-aortic balloon support with a

percutaneous left ventricular assist device in patients with revascularized acute myocardial

infarction complicated by cardiogenic shock. Eur Heart J 2005;26:1276–1283.

69. Kapur NK, Paruchuri V, Urbano-Morales JA, et al. Mechanically unloading the left ventricle before

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2013;128:328–336.

70. Seyfarth M, Sibbing D, Bauer I, et al. A randomized clinical trial to evaluate the safety and efficacy

of a percutaneous left ventricular assist device versus intra-aortic balloon pumping for treatment of

cardiogenic shock caused by myocardial infarction. J Am Coll Cardiol 2008;52:1584–1588.

71. Sassard T, Scalabre A, Bonnefoy E, et al. The right axillary artery approach for the Impella Recover

LP 5.0 microaxial pump. Ann Thorac Surg 2008; 85:1468–1470.

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73. Haj-Yahia S, Birks EJ, Amrani M, et al. Bridging patients after salvage from bridge to decision

directly to transplant by means of prolonged support with the CentriMag short-term centrifugal

pump. J Thorac Cardiovasc Surg 2009;138:227–230.

74. John R, Liao K, Lietz K, et al. Experience with the Levitronix CentriMag circulatory support system

as a bridge to decision in patients with refractory acute cardiogenic shock and multisystem organ

failure. J Thorac Cardiovasc Surg 2007;134:351–358.

75. Dembitsky WP, Tector AJ, Park S, et al. Left ventricular assist device performance with long-term

circulatory support: lessons from the REMATCH trial. Ann Thorac Surg 2004;78:2123–2130.

76. Takatani S. Progress of rotary blood pumps: Presidential Address, International Society for Rotary

Blood Pumps 2006, Leuven, Belgium. Artif Organs 2007;31:329–344.

77. Radovancevic B, Vrtovec B, de Kort E, et al. End-organ function in patients on long-term circulatory

support with continuous- or pulsatile–flow assist devices. J Heart Lung Transplant 2007;26:815–818.

78. Westaby S, Banning AP, Jarvik R, et al. First permanent implant of the Jarvik 2000 heart. Lancet

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magnetic bearings. Artif Organs 2006;30:324–338.

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arrhythmias. J Heart Lung Transplant 2007;26:819–825.

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a translation from pump mechanics to clinical practice. J Heart Lung Transplant 2013;32:1–11.

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89. Slaughter MS, Pagani FD, McGee EC, et al. HeartWare ventricular assist system for bridge to

transplant: combined results of the bridge to transplant and continued access protocol trial. J Heart

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heart. Ann Thorac Surg 1999;68:698–704.

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bridge to transplantation. N Engl J Med 2004;351:859–867.

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*A comprehensive listing of abbreviations used is available at the end of this chapter.

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Chapter 85

Thoracic Aortic Aneurysms and Aortic Dissection

Ravi K. Ghanta and Gorav Ailawadi

Key Points

1 The risk of thoracic aneurysm disease increases with age. Thoracic aortic aneurysms in young

patients are most likely due to genetic predisposition or familial syndromes.

2 Careful planning by experienced centers is paramount to provide optimal treatment in patients with

thoracic aortic aneurysms as the morbidity and mortality for surgical intervention are significant.

3 Open surgical repair remains the mainstay for aortic root, ascending aortic, and aortic arch

aneurysms with very acceptable outcomes and low morbidity when performed in centers of

excellence.

4 Endovascular techniques for the descending thoracic aorta have become the preferred treatment

approach not only for aneurysms, but for dissections and acute traumatic aortic injuries as they often

can be performed with less morbidity than that associated with open surgical treatment.

5 Aortic dissection is associated with higher operative morbidity and mortality. Stanford type A aortic

dissection mandates emergent operation. Stanford type B aortic dissection may be managed

medically if uncomplicated or with endovascular therapy if complicated. Management is evolving

with advancements in endovascular techniques.

Aortic diseases constitute the 13th leading cause of death in the developed world. Aneurysms can affect

the entire aorta, but aneurysms of the thoracic aorta, in particular, are associated with the highest

morbidity and mortality (Fig. 85-1). An aortic aneurysm is defined as a dilation of the diameter of at

least 50% greater than baseline. True aortic aneurysms affect all the layers of the aortic wall – intima,

media, and adventitia – and should be distinguished from false aneurysms (pseudoaneurysms), which

occur after trauma, surgery, or other injury and only involve the media and adventitia. Although

understanding of the pathogenesis of aortic aneurysms is rapidly evolving, degradation of the aortic

extracellular matrix proteins, collagen and elastin, and loss of smooth muscle cells are hallmark

pathologic findings. In contradistinction to abdominal aortic aneurysms, ascending aneurysms less

commonly display manifestations of atherosclerosis or an inflammatory infiltrate.

Thoracic aortic disease is associated with significant risk primarily due to catastrophic rupture or

dissection. Aortic dissections are intimal tears resulting in blood propagating within the medial layer,

leading to true and false lumens of blood flow. False-lumen perfusion can lead to visceral organ

malperfusion. Although dissections most commonly occur in aneurysms, dissections can also occur in

nonaneurysmal aortas with connective tissue or other aortic wall pathologies. Chronic aortic dissections

can also become aneurysmal over time, necessitating intervention. Treatment decisions concerning

operative intervention in terms of both timing and extent of resection are often complex and involve

multidisciplinary management (Fig. 85-2).

THORACIC AORTIC ANEURYSM

History

The first known description of an arterial aneurysm was by Galen, a Greek physician (A.D. 126–216),

who described false aneurysms in injured gladiators.1 In 1543, Andeas Versalius first described thoracic

aortic aneurysms (TAAs). However, it was not until 1895 that an etiology for aneurysms was

hypothesized, when Dohle identified syphilitic aortitis.2 Aneurysms were originally treated with

external or internal ligation via opening the aneurysm. In the later 19th century, Rudolph Matas

developed an alternate technique of obtaining proximal and distal control, aneurysm resection, and

primary reconstruction.3 These techniques were successful in only a limited number of patients.

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The modern surgical treatment of aortic disease began in the 1950s, and the ensuing 20 to 30 years

saw the development and failures of many novel techniques.4,5 In the early 1950s, the first resection of

a descending thoracic aneurysm and replacement with homograft was reported. In 1952, the first

excision of a saccular ascending aortic aneurysm without cardiopulmonary bypass was performed by

Michael DeBakey and Denton Cooley in Houston.6 In 1953, Dubost et al. in Paris and DeBakey and

Cooley in Houston reported successful resection and reconstruction of the abdominal aorta with human

aortic allograft.7,8 The same duo performed a repair of an acute traumatic aortic transection in 1954

through a left thoracotomy with the patient’s core temperature reduced to 28°C using surface cooling.

They subsequently reported the first successful resection of an ascending aneurysm with

cardiopulmonary bypass in 1956 and the first successful arch aneurysm repair in 1957.9,10

Dacron grafts, introduced by DeBakey, largely replaced human allografts, avoiding the need for

maintaining large tissue banks and allowing more facilities the ability to treat these patients.11,12 In

addition, the development and refinement of the cardiopulmonary bypass machine, in large part by

John Gibbon at Thomas Jefferson, revolutionized the open surgical repair of thoracic aortic disease. The

importance of hypothermia for cerebral protection and specifically the use of hypothermic circulatory

arrest (HCA) during aneurysm repair was established by Randy Griepp and colleagues.13 Advances in

endovascular therapies, led to the development of thoracic aortic stent grafts in 1994 by Michael Dake

and colleagues.14 With these techniques in place, modern surgical practice to treat aortic disease was

established.

Figure 85-1. Normal anatomic aortic segments. The aortic root extends from the aortic annulus to the sinotubular junction. The

aortic root is the largest diameter section of the aorta when measured at the level of the sinuses of Valsalva. The tubular or

ascending segment of the aorta begins at the sinotubular junction and extends to the innominate artery. The aortic arch travels

anterior to posterior and the left, giving rise to the head and upper extremity vessels. The descending thoracic aorta begins distal to

the left subclavian at the level of the ligamentum arteriosum to the pulmonary artery (PA). The abdominal aorta begins at the

level of the diaphragm.

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Figure 85-2. A: Sagittal CT scan showing an ascending aortic aneurysm. Computed tomography (B) and angiogram (C) of a patient

with a fusiform descending thoracic aortic aneurysm.

Table 85-1 Risk Factors for Thoracic Aortic Aneurysms

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